Scottish Doctor, author, speaker, sceptic

The planet Vulcan

I love reading about the history of science. In part, because I think you can learn so much about the process of thinking itself. Especially when it goes wrong. More especially when you are looking at the process of immunisation.

Immunisation is something that Karl Popper was particularly interested in. Popper was a scientific philosopher who is a bit of a hero of mine (when I can actually understand what he is saying). Amongst many other things, he was interested in the techniques used by scientists to protect favoured scientific hypotheses, which he called ‘immunisations’.

An immunisation is essentially a way of explaining why a fact, which appears to contradict a favoured hypothesis, does not actually contradict it at all. For example, when it was found that the orbit of the planet mercury could not be explained by classical Newtonian physics, a mathematician called Le Verrier postulated that there must be another, smaller, planet inside the orbit of Mercury that was affecting Mercury’s orbit. The planet Vulcan.

Vulcan was invisible – primarily because it did not exist. But for many years the invisible and non-existent planet served its purpose. It protected classical Newtonian physics from a potential contradiction, or refutation. Or, to be more blunt, of being simply wrong. In this case, scientists were quite happy to believe in invisible non-existent things, if the alternative was to cast aside a hallowed hypothesis.

Of course, this is just one of thousands of examples whereby unwelcome facts have been simply swatted aside, or immunised against. It is not just the Catholic Church that refuses to look through telescopes.

Vulcan, although just one example, does provide a good case study of a widely used form of immunisation tactic, the ‘ad-hoc’ hypothesis. An ad-hoc hypothesis is a secondary hypothesis that is bolted on to the side of the main hypothesis in order to defend it, or protect it. A more recent example of this can be seen in the Global warming debate.

It has been noted that global temperatures have not increased by much, if at all, in the last 15 years. This, however, is not viewed as a contradiction to the hypothesis of man-made global warming. Why not? Because it is argued that the oceans are taking in the excess heat, and trapping it. This process has held back the degree of global warming that had been predicted by the experts.

I am not going to debate whether or not this is true. I am just using it as a more recent example of an ‘ad-hoc’ hypothesis which came into existence to protect the central hypothesis. I would further add that ad-hoc hypothesis are not always wrong. They can very often be right. Le Verrier, prior to inventing the planet Vulcan, had predicted the presence of the plant Neptune due to irregularities in the orbit of Uranus.

However, if you read his works, you will know that Popper was not a fan of ad-hoc hypotheses. He felt that a good hypothesis should be fully predictive of future ‘events’ without the need for additional explanations, adaptations, or suchlike.

He did not state how many ad-hoc hypotheses it took before you had to admit defeat. One, ten, a hundred, a thousand? No-one can give you a clear cut figure, but the more of them there are, the less likely it is your central hypothesis was correct in the first place. The phenomenon of adaptation/immunisation had been recognised many years before Popper.

‘A nice adaptation of conditions will make almost any hypothesis agree with the phenomenon. This will please the imagination, but does not advance our knowledge.’ J Black 1803

I have recently been pondering the ad-hoc hypothesis once more in relation to heart disease. For I suspect that never in the history of science has a central hypothesis had so many ad-hoc hypotheses bolted on to it. Indeed, we have now reached the point where ad-hoc hypotheses have had ad-hoc hypotheses bolted onto them, to protect the ad-hoc hypotheses themselves from being refuted.

Just to look at one example. There are a number of drugs that have been developed to raise High Density Lipoproteins (HDL), the supposed ‘good’ cholesterol. A few of them also lower LDL ‘bad’ cholesterol at the same time. Billions have been spend on this class of drugs known as ‘trapibs’ . The first of these was Torcetrapib.

At this point I should probably remind you that the ‘good’ cholesterol hypothesis was only created as an ad-hoc hypothesis to explain why some/many people with high total cholesterol levels do not suffer from heart disease. ‘It’s because they have a high HDL level.’

The logic here was obvious, if horribly facile. Raise the HDL and reduce the risk of heart disease. Anyway, ignore the chasms of logic, along came the ‘trapibs’, which were going to take over from statins:

‘Hailed as a potential blockbuster that could take Lipitor’s place, torcetrapib was a cholesteryl-ester transfer protein inhibitor (CEP-T inhibitor) designed to increase good cholesterol and lower bad cholesterol. Development of the drug began in 1990 with clinical trials starting nine years later. But it wasn’t until 2006 that Pfizer got close to submitting the drug to the FDA. The company touted torcetrapib as the answer to its near-term pipeline woes, predicting the potential blockbuster could make up for billions of dollars in lost Lipitor sales when that drug went off patent in 2011.’

Well, torcetrapib certain raised HDL by about 50%, and lowered LDL by about 10%. So, what could possibly go wrong?

‘What went wrong: In late 2006, the walls came crashing down around the company. Pfizer announced in December that it was halting development of it’s prized Phase III asset. The decision came after an independent Data Safety Monitoring Board recommended terminating the study because of an imbalance of mortality and cardiovascular events. Results from a 15,000-person trial showed that patients taking torcetrapib with Lipitor experienced excess deaths than those taking Lipitor alone. Not long after torcetrapib demise, Pfizer announced that it was cutting 10,000 jobs. The company spent $800 million developing the drug.’ http://www.fiercepharma.com/special-reports/pharmas-biggest-flops/torcetrapib-pharmas-biggest-flops

What went wrong was the Torcetrapib increased cardiovascular deaths about around 50% (relative increase in risk). Several other ‘trapibs’ have since come, failed, and slunk from the playing field, taking many billions down the drain with them. Yes, I know, you have never heard of them. At the risk of sounding rather big-headed, I predicted their total and abject failure long before the results of the clinical trials came out.

Now, there are those of us i.e. me who would suggest that this blows a hole in the entire good, bad, cholesterol hypothesis. But no. Why not? Because it was found that torcetrapib raised the blood pressure, and lowered potassium levels. This, it seems, was enough to explain the massive rise in CV mortality. Well, quite reasonable, you might say. Yes, but the rise in BP was minute, and the drop in potassium was equally minute. This could explain, perhaps, a 5% rise (at most) in CV mortality. Which should have been overwhelmed by the massive rise in HDL, and drop in LDL.

But no-one was going to look too closely into the figures themselves. An ad-hoc hypothesis had been found. The ‘experts’, rather than questioning the central good/bad cholesterol hypothesis simply bolted on the ‘BP rise, potassium falls’ ad-hoc immunisation device and moved on.

So, here we have an ad-hoc hypothesis, bolted onto an ad-hoc hypothesis, bolted onto the central hypothesis. We have another planet inside the invisible planet Vulcan, to explain why it is so difficult to find the planet Vulcan.

As you can see, the games played to protect the cholesterol hypothesis are, literally, endless. I am not sure when the games end? Perhaps they never do. Very clever people, given enough time and money can, it seems, twist reality round and round, inside out and upside down forever. I would call the process vulcanisation, but I think that has something to do with rubber.

80 thoughts on “The planet Vulcan”

My own pet hate on global warming is that heating water releases CO2. We have a cause heat and its effect CO2 release. How can you reverse a cause and its effect in science? That makes it junk science along with all perpetual motion machines.

At the risk of jumping in without knowing if ferretman555 will reply, I think he means that, as it is an established fact that warm water holds less dissolved CO2 than cold water, it is impossible to claim a unidirectional causative link between rising CO2 levels and rising atmospheric/oceanic temperatures when rising temperatures will cause release of CO2 from the oceans to the atmosphere….
But as you say, it is not an argument to be plumbed too deeply here.

This is known as “knowing a tiny bit of science, and making it into a big deal”.This happens a lot, and most importantly when people shout about how something is predicted by “the first law of thermodynamics”, but they don’t know that there are four laws of thermodynamics. In simple terms, suppose that someone knows only one of the “rules of safe driving” and claims to be a safe driver because he/she knows this one rule, and follows it religiously.

Heating water decreases the solubility limit of CO2 in water, as well as any other gas.

If, the water were already SATURATED with CO2 at temperature T1, then raising the temperature of water to T2 would cause a release of CO2.

However, if the water were NOT SATURATED with CO2, then raising the temperature a small amount would not cause the release of CO2. The water would just heat up. Eventually, if you continued the heating of the water, you would likely reach a point where the solubility limit would decline so much that the water would then be saturated, and CO2 would be released.

I believe that ferretman555 has given us an excellent example of a “Junk Scientist” who knows a tidbit or two and doesn’t know how to actually apply it. I am grateful for someone to be so willing to display their understanding of science in the way that was done.

Global warming – now I know a bit about this, as I have tried modelling it myself – in that I have tried to physically determine how much warming you should get from a given increase in CO2 and methane.

My finding is that doubling CO2 and CH4 levels should give about 2 degrees of warming. There are numerous feedback effects that are possible, however the basic premise of global warming is solid science, it is just the excessive predictions that aren’t.
In terms of global warming stopping over the last 10 – 15 years, I think it tells us very little. During the 1990s global temperatures shot up for unknown reasons, maybe climate scientist tried attributing it all the greenhouse gasses, and that is why stagnation of temperatures is now a little embarrassing. However, based on the increases in GHGs over the last ten years, the predicted warming from this is always going to be below the threshold of statistical analysis.

As for oceans suddenly buffering temperature rises – I don’t know why anyone would propose this as there are so many flaws with this. Certainly oceans will buffer temperatures, they do this seasonally and diurnally, it is the reason why Scotland is green most of the year and not white! However, ocean buffering can only reduce warming, not stop it, and if they buffer temperature rises now, then they should have also buffered them during the 1990s.

The main problem with ocean buffering global warming, is that Greenhouse gasses drive warming from the atmosphere, so they need to warm the air before that temperature can be transferred to the ocean, so you can think of it like having a small bathroom with a fan heater in it. Try turning on the fan heater with the bath empty and seeing how quickly the room warms up, then try again much later with the bath full of cold water. Despite the fact that the cold water bath has far more heat capacity than the air, its effect as a buffer is quite minimal as the transfer of heat to the cold water is so slow.

So, certainly, a bit of skepticism towards global warming is in order, as claims do get out of hand, however just remember, the last 15 years of data neither disprove or prove global warming. There is really no need to apply a patch theory unless your warming model was predicting way more warming than it should have been!

Well since the JNC 8 guidelines don’t even recommend monitoring cholesterol, just to put people with risk factors on a statin and leave it at that, I suspect they are starting to realize that any benefit statins give is due to reducing inflammation, not reducing LDL.

One of the biggest issues with the development of any drug is that typically only one pathway is studied, like the inhibition of CETP and only its effect on LDL and HDL. More often than not, any given enzymatic pathway had effects on multiple systems, not just one. Of course, pharmaceutical companies don’t see any advantage to thoroughly investigating the entire picture.

Given my family history of CVD, I’m betting on niacin, which I’ve taken for 11 years. Combine that with a healthy diet, free of industrially processed food-like substances and moderate exercise, I’ve managed to become the first male in my family to not have a heart attack or stroke by the age of 50.

My former cardiologist, who prescribed added simvastatin to my niacin regimen, was adamant about placing me back on it after I had to discontinue both due to elevated liver enzymes. I chose to restart niacin and not take simvastatin. He was adamant about starting me back on a statin since my LDL was too high (i.e. 80 mg/dL or 2 mmol). I pointed out that there’s never been a single study showing that lowering LDL reduces heart disease. He reluctantly agreed and mumbled something about pleiotropic effects. I then pointed out that my HDL had increased from 30 to 52, without any niacin, with just a simple change in my diet. We still insisted.

I fired him. Two years later, I had a second EBCT which showed a decrease in my calcium score. I’m sure if I went back to the first cardiologist, he would still insist his way was the right way, even in the face of conflicting evidence.

I have a quick method of determining a medical professional’s judgement. I ask them for a scientific rationale for why they suggest a course of treatment. If they say it’s because of some committee’s recommendation, I automatically consider their judgement very suspect. I also enjoy asking them what the absolute risk reduction is of any given drug treatment if they cite the relative risk reduction. I have yet to receive a direct answer to that question.

If memory serves you originally used “ad hoc, unsupported hypotheses”; unsupported because there was no supportive scientific evidence. One wonders whether “theory” might have been more appropriate,

I also seem to remember that Prof Stephen Hawking once said that an hypothesis stood until one set of data arose that did not fit the existing hypothesis; a new hypothesis had then to be constructed.

This does not appear to be the case in the medical establishment supported research. In this case data is manipulated, modified or simply “disappeared” until it fits. In short it has been “doctored” to suit.

Another example was the “Epidemic of Congestive Heart Failure” trumpeted by the US NHBLI and CDC; now it does not exist on either website. It used to be on the THINKQUEST website but has now been archived. I have been told by an American cardiologist that the epidemic in the US is alive and well despite its now non-existent state according to the NHBLI and CDC. The rise was following sales of cholesterol lowering drugs!

Hi, Ed! I’ve recently been prescribed gabapentin for, ahem, women’s things. My doctor explained that it’s an anti-convulsant, often prescribed to epileptics, and also a painkiller, often very effective for neuropathic pain, and indeed, my mother takes it for this latter reason. He said that it is also often effective at banishing hot flushes, which have been the bane of my life for a while, now. I think this is a good example of a multi-tasking drug, especially as my hot flushes are already beginning to reduce in number, only two weeks after starting to take it. My doctor pointed out that side effects are possible, and what those might be, but so far so good for me. He also said that if I wasn’t happy to try it, he’d respect that, and we could discuss other options to help my symptoms. He said that HRT is not now instantly recommended – I’d told him I wasn’t really that keen, at this stage, to go down this path. At least he listened to me – as you were pointing out in your post, your first cardiologist didn’t seem remotely open to different options, or even to listen to what you were saying. Dr Kendrick – an excellent article, as always, and as a lifelong Star Trek fan, I loved the “Vulcan” bit!

I refer back to your articles on statins and my decision to come off them and, further my comments on the effect they had on me. It is now about a month since i stopped using statins and my energy levels have continued to rise, my libido has improved immeasurably and the fogginess has gone. I can only thank you for your articles and information that enabled me to make a mature decision about what medication i elect to take.

MK, I fully agree with your (beautiful) analysis. However in the case of the planet Vuclano the hypothesis presented by Le verrier caused no harm to humanity. On the contrary, the insistence on the idea that the bad cholesterol causes heart disease, in addition to not fix the problem is causing thousands of deaths.
Incidentally, the idea of ​​”good” and “bad” cholesterol is as scientific as the archaic idea of the struggle between “good” and “evil” that primitive peoples used to “explain” the natural and social phenomena.

I love this bit: ‘Results from a 15,000-person trial showed that patients taking torcetrapib with Lipitor experienced excess deaths than those taking Lipitor alone.’ How many deaths can one patient suffer before the drug is declared unsafe?

I think you have hit the nail right on the head! The practice of adding extra hypotheses to a theory just to keep it afloat is very misleading, and seems to have become extremely common across science.

Think for a moment about a typical elegant spiral galaxy. They are typically billions of years old and will have rotated a number of times since they formed. If their stars simply rotated under Newton’s laws of motion, the situation would be analogous to the solar system – where the distant planets rotate much more slowly than those nearer in – which would mean that all the nice spiral structure would soon get smeared out! If Newton had known about spiral galaxies, presumably he would have tried to modify his law of gravity to take this into account. Modern science’s solution has been to postulate ‘dark matter’ that changes the motion of the stars in a galaxy in a way that manages to keep the galaxy rotating in step and preserve General Relativity (which would also predict a smearing out, like Newton’s laws do). Just as you point out that the BP/potassium excuse for torcetrapib’s failure is too weak to explain the observations, dark matter is a lousy excuse for the failure of Newton’s laws (or General Relativity) applied to galaxies – because you would need just the right amount of matter in the right distribution to obtain the effect!

The Global Warming ‘science’ is indeed another good example, because after watching a slight temperature rise over the 80’s/90’s, followed by no further rise, you have to ask why the oceans would suddenly start to absorb the extra heat, when they didn’t do before! It might also be interesting to ask exactly how stable the global temperature could be expected to be – I mean the observed rise was less than one degree C, and the sun is not completely constant. Moreover, long before we had industry, there were ice ages followed by warming periods!

My impression is that modern science is chock full of this bogus thinking – probably because modern science is managed so ‘well’ nowadays by politicians and bureaucrats.

Science seems to have changed over my lifetime, and now it is more like the Catholic Church. It has become incredibly rigid, and has even invented its own version of morality (low carbon, statins, low fat, …..). I hope the bad science bubble bursts soon.

Excellent commentary. The up and coming ad hoc bolt-on to the cholesterol theory seems to be that the number of LDL particles is what actually causes heart disease and that conventional cholesterol labs are “risk factors” because they imperfectly correlate with LDL particle number. Many very smart and usually skeptical people such as Peter Attia seem to believe that this particle number ad-hoc hypothesis is finally the real deal. As far as I can tell, all they have to back this up are the usual associations with CVD, albeit stronger ones than standard cholesterol labs. Yet many seem convinced causality has been established. I’d be very curious to hear Dr. Kendrick’s take on all this.

Ad-hoc hypotheses tend to prosper most when the primary hypothesis is considered dogma and those who even *remotely* challenge the central theory tend to suffer for their presumption. A rational person would agree you have done no such thing here but I’m still interested to see how this thread plays out now that it has been mentioned by Judith Curry and brought to the attention of a particular audience…

Just looked her up. If she wants to take offence at my example, so be it. I normally stay well clear of the climate science debate as I don’t know enough about the science to make any useful contribution. I do, however, find the tactics very familiar. Ignore the skeptic, attack the skeptic, accuse the skeptic of having a financial interest in the matter, use incomprehensible statistical analyses to prove – when you seem to have been contradicted – that you were right all along, create another ad-hoc hypothesis… etc. etc. Its a well worn path. If a scientific hypothesis is right it should be accurately ‘predicitive’. Not much point in it otherwise.

I had an argument with someone not so long ago about this exact thing. My position was identical to yours. I don’t know about climate science, and I don’t have an opinion on global warming either way, but the treatment of the skeptics didn’t seem scientific to me at all. I was just met with, “You should side with the experts you fool!” This from friends who all claim to like science, they might like it but sometimes I worry they don’t quite get it. I’ve seen so many smart people mistaking politics for science I worry we’ll never get to the truth.

A true scientist (in my humble opinion) must never become too highly attached to any hypothesis. This, however, is very tricky. I find myself immediately looking for flaws in papers the support the ‘cholesterol hypothesis.’ Equally I find papers criticizing the cholesterol hypothesis make me feel well regarded towards them, and I am much less likely to look at them critically. I try not to do this, but I do. I mean, were I to be proved wrong in my belief that cholesterol has nothing to do with heart disease, then I would feel very foolish, but my entire existence does not rest on proving, or disproving, the cholesterol hypothesis. My income is almost completely unrelated to my writings (unfortunately). But if I were an International ‘expert’ on global warming my status, my income, my sense of self would be intimately dependent on one hypothesis. So, I can see why those who support the man-made global warming hypothesis lash out at people who disagree. I don’t think it is right, but I can understand it. The problem compounds when we defer to ‘experts’ and fear to question them. That is a very unhealthy situation indeed. Science needs to be a dispassionate discussion about the facts, wherever possible, or it no longer science.

I can’t speak for Judith Curry, but I suspect she agrees with your opinion on bolting ad hoc hypotheses onto hypotheses. To date, there has been 39 hypotheses put forward as to why there has no observed temperature increase for the last 10 to 18 years. (different temp data sources give differing results. Another issue,of course)

Judith is a very highly respected climatologist, who is very much against the “consensus” notion of science, and has been much vilified by some of the major players, such as Mike Mann, for daring to speak out against the “consensus”.

In this case Judith is the skeptic but there exists a troop of individuals who tend to dislike anything she says or anyone she tacitly endorses, hence the heads up.

I 100% agree that truly scientific hypotheses have predictive skill as well as the attribute of falsifiability. I read a message the other day (apologies to the author but I’ve forgotten where I read it) that when it comes to climate science the goalposts are moving around the field faster than the players at this point!

Nick. I tend to support anyone who takes on the entrenched ‘experts.’ I think it is critical that all scientific hypotheses are subjected to as much criticism and ‘attack’ as possible. If they withstand such assaults, they are probably right. The problem is, normally, the failure of the experts to engage in scientific debate, they tend to attack any criticism as a personal affront.

OK 4 years late but here’s my 2 cents. Looking at that page the criticism of Dr Kendrick is not coming from Judith Curry but from a commenter calling herself Susan Oliver. Judith merely linked to this post. As a trenchant critic of the Anthropogenic Global Warming thesis and it’s many bolt-on hypotheses to explain away its many failings and it’s proponents complete disregard for real-world data I suspect Judith wholeheartedly agrees with Dr K.

The practice of repeatedly trying to fix an inadequate theory has a very long pedigree indeed – people have probably been doing it as long as there have been theories. “If you wear this necklace, you will be safe from lions”. “My husband wore your necklace, but a lion ate him”. “He must have worn it the wrong way. Maybe a second necklace is necessary”.

Studying History of Science at school, 50 years ago, we were introduced to the Ptolemaic Theory of the Universe – in which the Earth was at the centre, and all the heavenly bodies (Sun, Moon, planets, stars) went round it in circles. To fit the model to the observed movements of the heavenly bodies (sic) an elaborate system of “epicycles” was cooked up. As a result, “To summarize, Ptolemy devised a system that was compatible with Aristotelian philosophy and managed to track actual observations and predict future movement mostly to within the limits of the next 1000 years of observations”. (http://en.wikipedia.org/wiki/Geocentric_model)

I remember this style of “adding a bag on the side” of an inadequate model was technically called “saving the phenomena”. As the phenomena were perfectly OK, and needed no saving, it should perhaps have been referred to as “saving the theory”. Obviously, it’s profoundly disreputable – especially since 1200 AD.

I have just returned from a visit to the local lipid clinic (always a joyous occasion). I am 37 years old and my total cholesterol is currently in the mid 7s and my triglycerides are around 8. I took a statin around 6 months ago but they gave me sore legs so I stopped taking them. The consultant was not happy about this at all. He applied enormous pressure to make me start taking them again (albeit at a decreased dosage) but I refused. He now wants me to take fibrates and coQ10 together with Ezetimibe. I have read your book and understand the counter argument but it is very hard to maintain confidence in this stance when the supposed expert is sat in front of you explaining how dire your situation is. It feels like I am guaranteed to suffer a heart attack in the next 10 years. As a result, I am extremely worried about what the future may hold.

Also ask him just how bad that ‘soreness’ might get! Here are some reports from people who took Simvastatin – also known as Zocor. This was the drug I was given, and I seriously feared I might end up in a wheel chair before I realised the problem was the statin!

I asked my doctor a similar question. He was telling me about the risks of having a stroke or heart attack and suggesting statins. I asked him what the risk actually was and he looked it up on his computer. I forget what it was now, but I said “That’s not very high then?”. He reluctantly replied, “No I suppose it’s not” and dropped the subject!

A few years ago a Doctor working in East Sussex was quoted in the local press saying that if you took statins for 20 years you might live for 15 days longer. I do not remember
whether adverse side effects or quality of life were discussed.

I have searched (as no doubt you have) to find a study that showed a life extension attributed to statins (on a herd basis of course – individual claims are difficult to substantiate). I did come across one that claimed that regular users of ibuprofen lived longer than those who rarely or never used the drug.

I am damn sure that many attempts to prove life extension have been done and FAILED; otherwise they would have been the subject of conferences, press releases and major advertising.

Hi Paul.
I can suggest some questions you could place before your consultant at the lipid clinic.They questions would indicate the extent of the gap in his knowledge. The answers that I know he would not be able to return stem from facts that are well established upon an evidential basis, while people in very small numbers have knowledge of them. To point to the answers I would intentionally preview something that deserves development and greater exposure once developed. it doesn’t make sense to gift you with the questions that would knock the stuffing out of your consultant without that I can have you link to the answers. Once the preview is complete and in place I’ll have some pointers for you I can link to here. Your consultant is no expert on cholesterol or on the business of atherogenicity, that will soon become far clearer to you.
There is no need to worry. You will only add to your prospects of complications if you resume statin medication. Supplementation with multivitamins and minerals makes sense according to a plausible school of thought, and CoQ10 will do more good than any statin. A book by Cooney and Lawren, ‘Methyl Magic’, lends explanation and guidance that dovetails with the way evidence backed facts have had my thoughts trending.

“it is very hard to maintain confidence in this stance when the supposed expert is sat in front of you explaining how dire your situation is. It feels like I am guaranteed to suffer a heart attack in the next 10 years. As a result, I am extremely worried about what the future may hold.”

Of course if you go to a “lipid clinic” they are going to get you to manage your cholesterol and if you go to a Ford concessionary they will try to sell you a car.

I feel you Paul. It is hard to venture on your own and go against the whole medical establishment. It feels like walking a tightrope without a safety net. Life was simpler when the issue was left to doctors and experts and all you had to do is follow their advice and not worry about a thing. The safety net was there, at least it seemed to be. But if the experts are wrong then the safety net was nonexistent, a mirage, a lie.

If Cholesterol is not the bad guy then what? What do you do with the numbers LDL/HDL triglycerides? What does it mean (if anything) to have higher (or lower) cholesterol than normal? And, what is normal? what can you do to improve your heart health? If the answer is not the statins or avoiding fats, then what?

There are no easy answers to those questions, because the scientific community at large (with exceptions) seems to be distracted in the wild goose chase of cholesterol. So they are not a source of answers and perhaps they never can be for the layman person, because in science answers are rarely definitive or clear cut. The media makes it seem as if science is black or white and it has all the answers but really there is little certainty in science and a large part is conjectures, hypotheses not meant for public consumption.

In a way you are going to have to choose carefully your sources, form your own opinions, and make your own decisions.
Good Luck

The question you need to ask, is just how constant would you expect global temperature to be? Notice the vertical axis on the graph you posted – it covers less than one degree centrigrade! People used to believe – probably rightly – that the earth was still warming slightly from the last ice age, and nobody worried about it – indeed the real fear was, and probably still should be, the return of another ice age. Climate is clearly never constant – a few hundred years ago the Thames would freeze in winter!

When you look at those graphs, it is very important to realise that the measurements were mostly made from ordinary weather stations, producing data that was barely accurate to half a degree! The data was then averaged together. Over the years, some weather stations have been retired, and the temperatures they would have recorded are estimated by computer! The temperatures are also subject to further computer processing – known as homogenisation – that is supposed to correct for various effects, but is itself highly suspect. For example:

It is inconceivable to me, why anyone would even expect such data to be absolutely trend free given the way the data is collected, and the layers of computer processing that are applied afterwards!

The subject of Global Warming is very badly reported. For example, the next time someone tells you about the loss of ice round the North pole (which seems to be recovering anyway), ask then about Antarctica. Strangely that pole gets much less attention – even though CO2 spreads evenly through the atmosphere:

When you think about the deception and wishful thinking that seems to have gone into the entire diet/cholesterol/statin area, is it surprising that there are other areas of science that are equally poor?

David. I find this all very interesting, but I don’t think I can become a blog on global warning – I think there are lots of those. My interest in Global Warming (on this blog), is primarily to highlight the techniques used to silence debate. I find the parallels with the cholesterol/diet-heart hypothesis to be spookily similar. (Not really spooky I suppose, just similar)

Hah Paul, that’s nothing!
My total cholesterol is about 10 (ratios allegedly “very good” but can’t remember exactly what the LDL / HDL levels were), triglycerides <1.
I eat LCHF. (Whether that has a bearing on anything other than perhaps the triglyceride levels I don't know).

Am I in the slightest concerned about my cholesterol levels? Not one bit (except if they were low). Whatever the levels, they are what they are for a reason and will no doubt change (up or down) in the future.
Why would I want to mess with them?

MY GP, who seemed pretty laid back when I stopped taking Statins, has now returned to the charge. He’s nagging, I’m refusing – all very stressful! Are there actually any reputable independent studies at all that show a link between raised cholesterol levels and heart disease?

Paul Mather raises a real problem for us mere mortals. Do physicians EVER consider any other solutions beyond medication these days? My GP insisted that diet and lifestyle changes would offer not an iota of difference to my blood profile, but I dared to differ. I reckon I am correct in contradicting my GP, but it is so difficult for patients to follow their instincts. We certainly need a complete overhaul of the whole health system, because the way things are going, there appears to be precious few folks certified as healthy, ‘cos that doesn’t generate dosh!

I know it is possible to detect if someone has really given up smoking, and surely it should not be impossible to devise a specific blood test that correlates well with exercise levels! I’d imagine such a test might encourage at least patients to actually do some exercise!

A doctor I had years ago once refused to give me antibiotics for something, and I was quite miffed at the time. Now I’m grateful. At that time, most doctors put people on antibiotics at the drop of a hat. Now they appreciate it was not a good idea. Perhaps in future years they will look at the indiscriminate use of statins in the same way. It is perfectly reasonable to question your doctor therefore. They are only human after all. They have been wrong in the past and we can see from what we read on this blog that whilst they may be amongst the brightest of us, they are not immune to a spot brainwashing!

Thanks Dr K for your honesty by the way. It certainly is easy to be drawn only to those articles which support your own view, I find myself doing it myself. The very fact that you admit that, makes me trust what you say even more. You are one of the Good Guys!

As a layman, I think all I can do is to read as much as I can around the subject as possible to try and understand the issues concerning the cholesterol, diet, heart debate. I find I am much more persuaded by Dr Kendricks arguments as they are always backed up by study after study and links to research supporting this position, something which is sadly lacking from the other point of view.
My conclusion is that fresh air, excercise and a balanced diet is probably the best I can do to look after myself, and to steer clear of the medical profession and tests unless it is absolutely necessary.

‘Oxidative stress’ is the leading cause of atherosclerosis – and the several risk factors we been informed about feed into (or converge upon) this process. Being ‘stressed’, in one or more of several possible ways, raises levels of certain stress hormones and these hormones are big consumers antioxidants. The balance of availability of methyl groups these antioxidants would normally supply can be challenged when stress related demand for them rises .. .. and when that happens levels of reactive oxygen species (or free radicals) ever present in the background may rise.
There are several factors which can raise levels of hormones that compete for acquisition of methyl groups or that consume vital methyl donating antioxidants in other ways. Mental anguish, worry, fear and economic insecurity head the list, smoking and drinking may feature, and highly glycemic high carbohydrate diets likely lend adverse influence too. Saturated fats do not feed into this causal mechanism and likely help safeguard against it. There is also sleep to consider (we need plenty to maintain safer endocrinological homoeostasis), the effects of light (we do not always get enough dark), and it should be noted that the act of ‘earthing’ helps contribute to endocrinological homoeostasis with proven normalising effects upon levels of cortisol.
Endocrinology, relative methyl deficiency, and the notion of ‘oxidative stress’ link together sweetly to explain how environmental and epi-physiological risk factors can feed into one relatively common process that is the very business of atherogenicity (forming plaques) at the cytological level (the level of the cell whose viability is compromised). Sequenced correctly and strung together they answer the questions that should arise with concern for and ambition to explain the business of ‘convergence’. Few people in medicine have pondered the issue of ‘convergence’ so they’ve never asked the question(s) and placed an obstacle in the way of returning the answer(s). In the real etiology of heart disease and atherosclerosis cholesterol suffers attrition from the crossfire of oxidative stress. That attrition compromises the viability, performance, function, and expression of key cells present in arterial tissues.
This explanation breaks no rules of physics, biology, physiology, cytology, genetics, or the degree of significance and 3 billion-odd years of evolutionary provenance cholesterol has for all eukaryotic forms of life (eukaryotic includes us humans btw).
Moreover, there are levels of existence at which oxidative stress enforces the ever present rule of ‘entropy’. This ever present rule of entropy dictates both you and your automobile as examples have a useful life whose term is guaranteed to be finite, but can be shorter or longer according to the dose dependent attrition rate of accumulated oxidative stress. Entropy also explains that any appearance of a steady state is either illusion or delusion in just about any corner of facet of the universe.
In contrast the fat/cholesterol hypothesis breaks just about every rule we know of and runs quite counter to the real evidence. It does however meet the need for simplicity and brevity which does so appeal to most humans.

One of the quotes which makes the greatest sense to me, is from Jacob Bronowski in regards to University students, “It is important that students bring a certain ragamuffin, barefoot irreverence to their studies; they are not here to worship what is known but to question it.” I remind my son (on track to being a Medical Student) of this frequently.

…also a story I’ll paraphrase from Richard Dawkins, about one of his Oxford Dons: where a respected Professor attended a lecture on what had been the basis his life’s work. A lecture at which the young presenter proceed to disprove the theory on which the older man’s career had been based. At the end of the lecture, the older man walked down, shook the younger’s hand and (amidst applause) thanked him!

I really enjoy your interest in the philosophy of science. It tells me of a profound attitude towards an understanding why the whole field of medicine has turned into a dogmatic “religion” in the name of profits. My own interest in this field, which started five years ago, was driven by exactly the same desire as yours and Popper is here also my favourite philosopher (besides Schopenhauer) with Poppers posthumous work “The World of Parmenides” being the best I have ever read about how the “natural sciences” once came about, now more than 2000 years ago. (Hippocrates was by the way part of that true science.)

And I am scared, at the bottom of my heart, about what is now happening with this science, and as it seems, in most disciplines at the universities. Business may profit from science but will never pursue it per se.

Prof,
I do like your approach.
“the whole field of medicine has turned into a dogmatic “religion” in the name of profits.”

This is true and it derives, I believe, from the overuse and even abuse of epidemiological methods. Dr James LeFanu in his book “The Rise and Fall of Modern Medicine” deals with under his “Social Theory” section. These techniques, using very large numbers of “statistical units” (aka patients) are able to establish statistical significance to very small differences in the herd which then stimulate the prescription of drugs to huge numbers of patients within the herd; the vast majority of whom will not benefit. In short they ignore the probability of benefit to the individual!

With regards to Vulcan, I think you have been a little unfair. What was observed were perturbations to Mercury’s orbit, these could only be explained by an additional mass inside Mercury’s orbit generating an additional gravitational effect. They calculated the orbit of Vulcan, which would have been impossible to observe as it would always be in the glare of the sun, the only time that it could be seen would be in transit across the sun, this was calculated but never observed. They made an observation, created a hypothesis to account for the observation, but couldn’t verify the hypothesis. It wasn’t until Einstein produced his general theory of relativity that the perturbations could be explained. Mercury is so close to the sun that the energy from the sun’s gravitational field behaves like a mass generating its own gravitational field, using Einstein’s mass energy equivalence equation E=MC2, and it is this second order gravitational field that perturbs the orbit of Mercury. It is wrong to criticise the earlier scientists for creating a wrong model, there wasn’t any alternative. A similar story applies to the phlogiston theory of combustion.

I believe I was only pointing out how the process of ad-hoc hypotheses comes about. However, I would criticize scientists – always – for being too willing to believe in various ad=hoc hypotheses, rather than looking more critically at the central hypothesis itself. As for the perturbations in Mercury’s orbit, surely it is possible for scientists to have said ‘we cannot explain this.’ As Isaac Asimov said: ‘The most exciting phrase to hear in science, the one that heralds new discoveries, is not ‘Eureka!’ but ‘That’s funny…’ If you decide to immunize against ‘that’s funny’ observations, you can continually modify any hypothesis, but you are most likely moving further away from true understanding of the phenomena that you are observing.

“That’s funny”
Those paradoxical observations that defy the currently accepted dogma are real opportunities to advance science. They afford a rare and precious possibility of delving deeper into the mystery.

In those circumstances it is perfectly fine and reasonable for scientists to develop ad-hoc hypothesis but then they need to be either verified or disproven at every opportunity, not just accepted as truth because is convenient. The purpose of an ad-hoc hypothesis should never be to “save” a previous hypothesis but to challenge the accepted notions with new ones. They in turn must be treated with the same distrust as any new hypothesis, meaning until some verifications have been made they are nothing more than an idea. They should never get a pass just because they support or “save” an already accepted theory.

That’s funny!
“Those paradoxical observations that defy the currently accepted dogma are real opportunities to advance science. They afford a rare and precious possibility of delving deeper into the mystery.” Sadly they are so often ignored.

1913 saw the reporting of positive induction of atherosclerosis following administration of cholesterol to the rabbit through the doctoring of feed. This led Keys in the post-war era to hypothesise that cholesterol might be the dose dependent atherogen at work and giving rise to positive indication. (It wasn’t actually) His hypothesis is the reason modest hypercholesterolemia in the human is considered by many to be the cause of atherosclerosis and a risk factor for heart disease. However exceptions apply at either end of the spectrum. Many admissions following a heart attack have ‘normal’ levels of cholesterol, while levels of serum cholesterol do not predict incidence of heart attacks that well either, and incidentally, homocysteine now looks to be very reliable in predicting prospects of outcomes associating with development of several chronic conditions. Keys thought hyopercholesterolemia had a cause and he hypothesised saturated fat would be the dose dependent factor driving hypercholesterolemia. I can see why a person might think fats in the diet might bear upon serum cholesterol levels and might be deserving of investigation, but Keys never actually investigated this, and he fudged a study in 1953 that implied saturated fats in the diet have angiotoxic properties. Yerushalmy and Hilleboe exposed the shortcomings and the abuse of data in 1957.
the confounding error in behind the 1913 result and also replicating it in other examples was exposed in 1976 by Hideshige Imai et al. Atherogenicity arises from certain oxides of cholesterol and not from cholesterol itself. This was established with more rigour in further experimentation that took up with the 1976 findings. In a book published in 1991 Peng & Morin reviewed the entire body of knowledge surrounding the biological effects of cholesterol oxides.
My copy of Peng and Morins book sat on the shelves of the Sheppard Library of the Mass. Col. Pharm, Boston, for between 12 and 19 years from 1995 and accrued just four date stamps. When it arrived with me it was in pristine condition. Now after three months in my possession it shows real signs of combat stress and attrition as I try to extract the content that most serves my campaign ambitions. Dr Kilmer McCully directed me to it.
Kilmer McCully is the only cholesterol sceptic author (I know of) to mention Hideshige Imai in passing. No other cholesterol sceptic authors can have read Peng & Morin or acquainted themselves with the biological effects of cholesterol oxides because if they had it would have shown in aspects of their work.
Rabbits did make for a poor choice of subject for the 1913 experiment, that’s true, but positive induction of experimental atherosclerosis was still a genuine result despite it was not the cholesterol itself what gave rise to it. From 1913 to 1976 interpretation of experimental atherosclerosis was blighted for not realising cholesterol oxides were present in the cholesterol administered, and even in the rabbit certain cholesterol oxides gave rise to genuine and consistent results. Experimental atherosclerosis, under the light of being alerted to cholesterols highly labile nature, is a result deserving of explanation, as opposed to being explained away (as is sometimes the case).
So now we know why some ethnic peoples can eat high fat diets and not get heart disease. The French, Alaskan Eskimos, Siberian Eskimos (Evenks), and certain African tribes eat high far diets without ill effect. The grisly bear is commanded by hromonal factors to go grossly hyperphagic (overfeed by a factor approaching consuming ten times more calories than is actually needed to meet the daily budget) as preparation for the enforced and total hypophagia of hibernation. What’s really odd (but isn’t actually) is that the bear becomes significantly hypercholesterolemic in the early days of hibernation when it isn’t actually feeding. “It isn’t yet understood how it can be that the bear can tolerate such high levels of cholesterol and yet not suffer heart disease”, ran the narration to the TV documentary that alerted me – or words along similar lines. It was an example of one of those, “That’s funny!” moments. And I’m thinking, “Yes it $%**^^!!-well is understood, cholesterol is not a dose dependent atherogen in any eukaryotic species !!” Science has established the fact. Peoples awareness of the facts are just a bit limited. And in many cases they are unaware their awareness of the facts might be a bit limited.

In the light of ad-hoc revisions to hypotheses people can overlook the very facts that should have them reshaping their cherished hypotheses. ” If you decide to immunize against ‘that’s funny’ observations, you can continually modify any hypothesis, but you are most likely moving further away from true understanding of the phenomena that you are observing”, and in the confusion that follows you diminish peoples capacity to identify with the truth even (long) after it emerges. Hypotheses owe a lot to consensus. Facts need evidence. Facts do feed consensus, albeit often quite slowly.

The fat/cholesterol hypotheis is dead: Long live the fat/cholesterol hypothesis!
Any impression of the steady state is dead, because the Universe and all that is within it must be evolving, including the nature of human ideas and the balance of evidence that supports them Despite this: Long live the steady state! – because we humans do so resent change, especially where it presents a challenge to our perceptions.

Thanks for a wonderful summary of the cholesterol hypothesis! However, even though I know infinitely less about this subject than either you or Malcolm K, I tend to side with him on the question of cholesterol oxides.

Although not meant that way, couldn’t cholesterol oxides be seen as yet another hypothesis glued on to the same rotten cholesterol theory? After all, cholesterol is just one of a vast array of chemicals in our bodies, and maybe it has nothing to do with promoting plaque formation – just as elastoplasts don’t cause skin abrasions!

Maybe someone knows why those rabbits got plaques, but has the work even been repeated? It might be a one-off, or maybe rabbits found their cholesterol laden feed particularly stressful, or was another additive needed to get the rabbits to consume their food at all? I started out in science myself, but by now I am absolutely amazed by how easily science seems to end up with the wrong end of the stick.

Having learned about the whole sorry episode of scientific muddle in this area, I think I’d need some very firm science to persuade me that anything other than stress and sugar causes most CVD’s. People seem to have an almost in-built urge to blame something diet related for these events – sin has to be involved somewhere!

As we have been discussing, science seems to have picked up some fairly irrational habits, and maybe one of them is to insist on replacing a failed theory immediately with another, rather than embrace a don’t know position for a while.

David,
“Maybe someone knows why those rabbits got plaques, but has the work even been repeated? It might be a one-off, or maybe rabbits found their cholesterol laden feed particularly stressful, or was another additive needed to get the rabbits to consume their food at all? I started out in science myself, but by now I am absolutely amazed by how easily science seems to end up with the wrong end of the stick.”
There is no mystique in how, in the case of the fat/cholesterol hypothesis, ‘science’ promoted by Dr Ancel Keys took up with the wrong end of the stick and ran with it. Experimental atherosclerosis has been repeated on several occasions and in several species. In vivo experimentaion has been conducted upon rabbits, chickens, squirrel monkeys, and, in a manner of speaking, the human. In vitro experimentation has been conducted upon cultures of tissues from further species. Experimental atherosclerosis remains a very genuine result. However the result itself and interpretation of the results can differ according to methodology used. Anitschkow and Chalatov (1913) positively induced atherosclerosis in the rabbit by feeding cholesterol, but cholesterol exposed to air will turn progressively rancid, and they did not know nor account for this in their adopted methodology.
The common autoxidation derivatives of cholesterol Peng & Morin listed in 1991 are:
Cholest-5-ene-3B,7a-diol
Cholest-5-ene-3B,7B-diol
3B-hydrosycholest-5-ene-7one
5a-cholestane-3B,5,6B-triol (or Cholesrtane-3B,5a,6B-triol, or cholestanetriol)
Cholest-5-ene-3B,25-diol (Common name 25-Hydroxycholesterol)
20s-Cholest-5-ene-3B,20-diol
5,6a-Epoxy-5a-cholestan-3B-ol
5,6B-Epoxy-5B-cholestan-3B-ol
3B,5-Dihydroxy-5a-cholestan-6-one
Cholest-4-3-ene-3-one
There are a total of 49 alternate and naturally arising first generation cholesterol oxides, and many of these may provide the provenance for further derivatives in the second generation. Peng and Morin direct many of these 49 oxides require enzymic cofactors in order to form. This indicates an air of legitimacy. If cholesterol oxides are involved in signalling feedback and operational control we ought no be so surprised because cholesterol is the foundation molecule from which all the steroidal hormones are formed.Steroidal hormones tinker with biochemistry and cytology sufficiently well to encourage sex but also account for the important tissue and morphological difference between male and female. Many cholesterol derivatives then are functionally expedient to the way our cells and we work. The ones listed above are those you might expect to form over time in a keg of stored cholesterol, or whose formation might be hastened by handling or heating as you add cholesterol to chow. They may well form under in vivo conditions.
Peng & Morin provide the many citations that charted the assimilation of knowledge surrounding cholesterols highly labile nature and its many naturally arising oxides. I must explain, scientific endeavours backed by pharmacological funding are investigating synthetic cholesterol oxides on account of their intended capacity to kill cells. The hope is that synthetic oxides of cholesterol can specifically target cancer cells. Crucially Peng, Morin and their contributing authors explain how the science now strongly implicates cholesrtane-3B,5a,6B-triol and 25-hydroxycholesterol as the leading cytotoxins from within the list above that are capable of promoting atherogenicity.
The whole purpose of my contribution to thread has been to say that the perceptions people have that cholesterol is an atherogenic agent is not supported by evidence – its origins are traceable to a confounding error. But experimental atherosclerosis strongly indicates the involvement of one or more atherogenic agents. What appear to be genuine results returned since 1976 indicate is that oxides of cholesterol, certain of them, return experimental atherosclerosis in vivo, and also indicate the necessary cytotoxic tendencies in vitro.
The original post was about the danger that accompanies ad-hoc revisions to hypotheses. The fat/cholesterol hypothesis has no shortage of ad-hoc revisions because aspects of it were never fully investigated at the outset and the supposed involvement of dietary fat as driving hypercholesterolemia was pure supposition. The six countries study was a fraud, and at the outset Dr Ancle Keys was led up the garden path by a confounding error. How plain need it be that the fat/cholesterol hypothesis and the case for lipid modification is based upon a complete absence of evidence? All that said experimental atherosclerosis still remains a consistent and genuine result deserving of reinterpretation. ‘Cause’ was wrongfully attached to ‘effect’ in the era before 1976 while the post 1976 era provided opportunity to reconsider the effect and reinterpret ’cause’.
What responses have shown is that ad-hoc dismissals pose as much of an obstacle to the rightful advance of science as can ad-hoc revisions.
If people took up with the recommended direction to read Peng & Morins book, ‘The Biological Effects of Cholesterol Oxides’ they would see there is significant body of peer reviewed accounts of experimental investigations in need of review before any person should rush to dismiss involvement of cholesterol oxides in atherogenicity.
Ad-hoc dismissals are something we do several times a day. News of events reaches us several times a day. Every event or eventuality about us has a cause, how many can we explain or even attempt to? We even concede there exists a gap in our knowledge but we so easily discount that important questions and answers may be placed within that gap. That ad-hoc dismissals arise so often in everyday life is the root of many a misunderstanding. In science ad-hoc dismissals prevent the scientist from seeing facts for what they are.

Surely the Vulcan hypothesis was a perfect example of bolstering a theory with an ad hoc hypothesis – postulating a planet that was to small and too close to the sun to be observed!

You can’t accept ad hoc hypotheses just because nothing better is immediately available because better theories come from anomalies, so if you cover up the anomalies for want of a better theory, it never arrives! Einstein might have read about Vulcan, and given up on GR!

The mass of ad-hoc theories over cholesterol must have delayed all sorts of science. For example, if people had recognised that reducing cholesterol or LDL/HDL was no use, someone might have figured out a molecule that produces the anti-inflammatory effects of a statin without the (no-longer wanted) cholesterol lowering effect.

Maybe we need a website that tries to keep track of unsupported hypotheses designed to save theories so that people can see at a glance those areas of science that might be wrong because they are encrusted in extra hypotheses!

I don’t think that scientists or indeed humans as a whole are content to say “we cannot explain this”, observed phenomena almost demand an explanation, this is how science in particular progresses. Most hypotheses start off as ad-hoc explanations of what is observed. The problem arises when eyes become blinkered and hypothesis/ theory becomes dogma to the point where alternatives are rejected without any consideration to their possible validity. This is what happened to the Copernican heliocentric view of the solar system, Galileo’s reporting of sun spots, and Kepler’s theory of elliptical orbits as these in different ways challenged the concept of a ‘perfect’ theocentric universe.

Malcolm.
“I do not agree with the oxidation hypothesis, however. As you might expect I know Kilmer quite well and very much respect his ideas.”
I am not convinced of the oxidation hypothesis either. Lessons arise when facts are established; often demonstrated by the ability to predict effect that should follow hypothetical stance upon a ’cause’. Hypotheses are what science works with before it can reliably reproduce cause and effect from which lessons can be learned.
Experimental atherosclerosis can be reproduced in several species and has been. You no longer do it by administering pure cholesterol, mind, because pure cholesterol is not atherogenic. And there forty-odd cholesterol oxides that have purpose in physiology that would not induce experimental atherosclerosis either. However as cholesterol oxides go cholestane-3B,5a,6B-triol and 25-hydroxycholesterol do seem to exhibit consistent cytotoxic tendencies backed by experimental evidence. I have not yet reviewed the original accounts Peng & Morin cite, but they do appear deserving of review.
As for Kilmer McCully I too respect his ideas and achievements. What is now known about the metabolism of homocysteine and the complications that associate with chronic hyperhomocysteinemia owes a lot to Dr McCullys’ efforts and tenacity in the face of of obstacles that the establishment placed in his way. Dr McCully has obliged me with courteous and helpful replies to email inquiries on at least two occasions. And something I find very appealing is that he provided the foreword to ‘Methy’ Magic’, a book by Cooney and Lawren. Craig Cooney populated the page with a lot of dots which he then joined to lend an image upon methylation, and methylation has its place in fat greater picture. McCully has devoted his career to doing the same for homocysteine.
There is a list of people I’d truly like to meet before I die. McCully, Graveline, Clinton Ober are high on that list, and so is one Dr Kendrick. The Great Cholesterol Con was the frost book I read on cholesterol and CVD. Then works of Ravnskov and Graveline must have followed. Graveline put me on to the work of McCully and soon I realised how these alternate works with alternate strengths and weaknesses and written in alternate styles augmented each other.
Something that impressed me greatly about the ‘Con’ is mention of psycho-social stress. Initially mention of this invited my scepticism (I had cheated and read the end first). But when I followed to discourse your argument won me over. But atherogenicity is a business which needs certain cells to be induced to behave badly or differently, and so physiological risk factors and those risk factors that are epi-physiological (such as psycho-social stress) must converge upon this process if they do genuinely play into it. Where Dr McCullys argument in the Homocysteine Revolution is especially strong and inspiring is that he discusses the issue of convergence of risk factors in relation to prospects of hyperhomocysteinemia. He does this naturally without mentioning the term ‘convergence’ and perhaps not realising the principle could be applied in other ways. Where your discourse is weak is that while you indicate epidemiological grounds to think of psycho-social stress as a casual epiphysiological risk factor for CVD is that you only trace ‘convergence’ as far as the HPA-axis.
Oxidation theory, methylation theory, homocysteine theory, and endocrinology surrounding the hormones of the HPA-axis all augment each other and, at least as I see it, augment your psycho-social stress hypothesis. In turn, by following up on a chance encounter with a sound-bite from Bernard Lietaer, I understand the real economic origins of pyscho-social stress perhaps better than you do.
The hypothesis surrounding certain oxides of cholesterol is far from confirmed because it remains a significant and unanswered question precisely when, where, and how, cholesterol may become oxidised to form (in the least) the tow prominent atherogens of its 49 possible oxides. Does homocysteine, a powerful oxidising agent and a notable zwitterion, contribute to the oxidation of cholesterol and does it result in the formation of the notable atherogenic cholesterol oxides, or does homocysteine merely indicate elevated levels of oxidative stress present within physiology? The latter is almost certainly true, but the truth could still extend to the first question. In otherwise healthy people homocystiene indicates elevated levels of oxidative stress running in the background that arise because too few antioxidant methyl groups are supplied to match demand. Almost inevitably levels and persistence of other reactive oxygen species (ROS) would rise in association with higher levels of homocysteine and damage by ‘free radicals’ would escalate as a feature of the ensuing ‘cascade’.
The conversion of norepinephrine to epinephrine consumes a methyl group, while the turnover of glucorticoids and cortisol is also reliant upon consumption of methyl groups. Ergo stress of various types that has bearing upon hormonal balance and homoeostasis has capacity to create added demand for methyl groups whose supply may vary but is nonetheless finite. One aspect of oxidative stress may pivot about the relative supply and demand of methyl groups, and rising homocysteine indicates a relative deficiency of supply of key methyl donating antioxidants that is not equating to demand.
Economic iniquity, psycho-social stress, disturbance to endocrinological homoeostasis, methyl deficiency, homocysteine, oxidative stress, and certain oxides of cholesterol do seem to form one of the plausible chains that can explain atherogenicty and satisfy the need to account for ‘convergence’ upon that very porcess at an endocrinological level.
Moreover the facets that can induce endocrinological disturbance and that may then elevate physiological demand for and consumption of methyl groups are several. They are a feature of mans world and do not necessarily feature ‘in the wild’. Moreover some of them have gained influence in the trend to modern, western, and civilised which can account for why remote peoples do not suffer the same complications as modern western civilised people do. Rubber-soled footwear and infrequent opportunities have a bearing upon oxidative stress and endcrinological imbalance, High carb diets do too, and people are exposed to unnatural sleep-wake cycles and are exposed to light when it ought to be dark. There exists evidence to have us realise these can influence the balance and levels of key hormones.
I do not claim the oxidation of cholesterol hypothesis for my own. But I do feel I navigated my way myself to arrive at inclusive view that others have indeed arrived at themselves and that did so before me. Stanford Field is one, Craig Cooney another, Patrick Holford and Dr James Braley are others. So long as we are guided by facts and are not misled by ad-hoc revisions – and so long as ad-hoc dismissals haven’t had us exclude some pertinent facts – there remains a a possibility that the way our thinking has trended might be on the right lines.
Genetics now tends to agree with and augment our view. The accumulated attrition of oxidative stress over the course of a life, even when kept to a minimum, is what most dictates the term of the most enjoyable and productive of lives must be finite and could never exceed the order of 110 years. Then genetic expression is guided more by methyl switches annexed to the genes that it is by the genome itself. There exists in the coding that is not active. Active genes can be switched off quite readily, and deactivated genes can be reactivated as readily by the mere addition or subtraction of a methyl group attached to the gene. Oxidative stress accounts for wear and tear upon telomeres that would otherwise preserve the integrity of chromosomes.
The attrition rate of oxidative stress is ever present at a basal rate but can be higher, in which case the life will be shorter. As with E=mc2 the basic principle(s) that nature adheres to is(are) disarmingly simple, while the ramifications can get very involved.
I respect your opinions upon cholesterol oxides but I think there are facts equally deserving of respect, and I think there are general principles at work that sit comfortably with facts that sit less comfortably with your opinions upon cholesterol oxides. Your scepticism did me a great service. It was the catalyst that had me email Dr McCully and his response that introduced me to the work of Peng & Morin.
Finally what about the plight of Korean and Vietnam war veterans? They had high incidence of arterioscleropsis and atherosclerosis. They were given combat rations in which powdered egg and powdered milk were a feature. Cholesterol is present in some food-stuffs and so must some cholesterol oxides. Traditional handling doesn’t actually invite so much autoxidation of cholesterol in food as one might anticipate, but production of powdered egg and powdered milk does (or did). The presence of atherogenic oxides of cholesterol were traced to the powdered egg and powdered milk that featured in these combat rations and featured in the explanation for the plight of of these veterans., or so I glean. In a sense in vivo positive induction of experimental atheroscloerosis include several species, rabbit, chicken, squirrel monkey, and HUMAN. Experimental atherosclerosis is a consistent outcome with a consistent cause that should not be dismissed, especially in the human.

Dr Kendrick cannot provide individual patient advice over the Internet. UK General Medical Council regulations are clear that to do so would be a breach of medical standards that could result in disciplinary proceedings.

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